The heart consists of two pumps. The right heart pumps blood through the lungs to the left heart which pumps the blood out to the rest of the body. The right and left ventricles are the pumping chambers for each side of the heart. The cardiac cycle is separated into two periods, systole and diastole.
Systole is the period in which the ventricles contract and eject blood into the aorta (left side) and the pulmonary artery (right side). As systole begins, an electrical signal spreads across the ventricles causing depolarization of the cardiac muscle cells. During depolarization, ions (sodium, potassium, and calcium) move into and out of the muscle cell. The right and left ventricles begin to contract and the blood pressure in each chamber begins to rise. When the pressure in each ventricle surpasses the pressure in its respective atrium, the valve between that ventricle and atrium closes, beginning the period of isovolumic contraction. The sudden stop of the movement of blood and the tensing of the ventricle around the incompressible blood results in the first heart sound (S1). During isovolumic contraction, the ventricular muscles continue to contract, causing the pressure in the blood to rise rapidly until it surpasses the pressure of the blood in the aorta or the pulmonary artery. At this point, the aortic and pulmonary valves open and blood is ejected. Pressure continues to build in the ventricles during the ejection phase until a point where the muscles stop contracting and begin to relax. This point marks the peak systolic pressure. In order for the cardiac muscle to relax, the cardiac muscle cells must repolarize with movement of ions through the cell membrane. As the muscles begin to relax, the pressures in the ventricles begin to fall until they drop below the pressures in the aorta and the pulmonary artery, causing the aortic and pulmonary valves to close. This ends systole and is marked by the generation of the second heart sound (S2).
Diastole begins with the isovolumic relaxation phase, during which all valves are shut. As the ventricles continue to relax, the pressures in the ventricles drop below the pressures in their respective atria. At this point, the mitral and tricuspid valves open and blood passively flows into the ventricles. During the passive filling phase, blood from the atria flows into and begins filling the ventricles. At the start of the passive filling phase, the ventricles are still relaxing and the pressures continue to drop, even though blood is beginning to fill the ventricle. Eventually, the blood pressure in the atrium and the ventricle become nearly equal and the blood pressure stops dropping. This is called ventricular diastolic pressure and is associated with the atrial filling pressure. Finally, the atria receive a signal to contract and a final bolus of blood is pushed into the ventricle before systole begins.
Ischemia is a leading cause of mortality and involves oxygen starvation of the myocardium. Once severe ischemia begins, it is critical that appropriate therapy begin within one to two hours in order to prevent severe damage to the heart muscle. Unfortunately, many episodes of myocardial ischemia do not cause excessive pain or other noticeable warning signs, and often go undetected. If left untreated, myocardial ischemia can lead to the symptoms associated with acute coronary syndrome and the eventual cell death associated with acute myocardial infarction. Acute coronary syndrome generally includes the clinical symptoms associated with unstable angina, non-ST segment elevation or non-Q-wave myocardial infarction, and ST segment elevation or Q-wave myocardial infarction. Early detection of myocardial ischemia provides the opportunity for a wide range of effective therapies such as surgical revascularization, neural stimulation, and drug delivery to reduce cardiac workload or improve cardiac circulation.
An electrocardiogram (ECG) or electrogram (EGM) presents a PQRST waveform sequence that characterizes the cyclical cardiac activity of a patient. The T-wave can be used to identify an ischemic condition. The ST segment, also associated with the repolarization of the ventricles, is typically close in amplitude to the baseline (i.e., isoelectric amplitude) of the signal sensed between consecutive PQRST sequences. During episodes of myocardial ischemia in the left ventricle, the ST segment amplitude deviates from the baseline. Accordingly, deviation in the ST segment is often used to identify an occurrence of myocardial ischemia.
Unfortunately, the use of the ST segment as an indicator of ischemia can be unreliable. The ST segment may deviate from the baseline due to other factors, causing false indications of myocardial ischemia. For example, the ST segment may deviate from the baseline due to changes in the overall PQRST complex, possibly caused by axis shifts, electrical noise, cardiac pacing stimuli, drugs, and high sinus or tachycardia rates that distort the PQRST complex. Consequently, the reliability of the ST segment as an indicator of myocardial ischemia can be uncertain.
In addition to the electrical activity of the heart, the mechanical activity of the heart (e.g., heart contractility), is affected during ischemic episodes. The term “contractility” generally refers to the ability of the heart to contract, and may indicate a degree of contraction. The dynamic mechanical activity of the heart can be represented by a heart acceleration signal or a pressure signal in order to provide an indication of heart contractility.
When a patient is experiencing chest pain or other sever symptoms, he or she eventually arrives at the emergency room after some amount of time. When the patient arrives at the emergency room, a twelve-lead ECG is used to measure the electrical activity of the heart. However, even a twelve-lead ECG has only about fifty percent sensitivity to acute myocardial infarction in the emergency room. When the patient arrives at the emergency room, cardiac biomarkers are also often measured. Cardiac biomarkers are substances that are released into the blood when the heart is damaged (e.g., troponin). The best biomarkers are chosen because the normal background concentration is near zero (i.e., anything above zero is abnormal), which leaves little room for error. Increases in cardiac biomarkers can identify patients with acute coronary syndrome, allowing an accurate diagnosis leading to appropriate treatment of their condition. Unfortunately, the biomarkers are released only once the muscle cells being to die and it can take about four to six hours for the biomarker concentrations to reach critical levels. By this time, however, many heart muscle cells would have died and the heart muscle would be severely damaged.
The symptoms of acute coronary syndrome include chest pain, pressure, nausea, and/or shortness of breath. These symptoms are associated with heart attacks and angina, but they may also be seen with non-heart-related conditions. In addition, these symptoms may be misinterpreted by the patient, leading to long delays before reaching the emergency department.
Heart sound monitors have also been proposed to detect ischemia. These heart sound monitors attempt to detect the S4 heart sound that is produced just after atrial contraction at the end of diastole by the sound of blood being forced into a stiff/hypertrophic ventricle. The S4 heart sound is a sign of a pathologic state, such as a failing left ventricle. However, the S4 heart sound is small and difficult to hear and its appearance does not always correlate to ischemia. Some people normally have the S4 heart sound while not experiencing ischemia.